ABSTRACT
Introduction: Noise-induced hearing loss (NIHL) due to industrial, military, and recreational noise exposure is a major, but also potentially preventable cause of acquired hearing loss. For the United States it is estimated that 26 million people (15% of the population) between the ages of 20 and 69 have a high-frequency NIHL at a detriment to the quality of life of the affected individuals and great economic cost to society.
Areas covered: This review outlines the pathology and pathophysiology of hearing loss as seen in humans and animal models. Results from molecular studies are presented that have provided the basis for therapeutic strategies successfully applied to animals. Several compounds emerging from these studies (mostly antioxidants) are now being tested in field trials.
Expert opinion: Although no clinically applicable intervention has been approved yet, recent trials are encouraging. In order to maximize protective therapies, future work needs to apply stringent criteria for noise exposure and outcome parameters. Attention needs to be paid not only to permanent NIHL due to death of sensory cells but also to temporary effects that may show delayed consequences. Existing results combined with the search for efficacious new therapies should establish a viable treatment within a decade.
Article highlights
The classical pathology of NIHL is destruction of auditory hair cells and degeneration of spiral ganglion cells.
Based on the molecular mechanisms of NIHL, therapeutic protection has successfully been developed in animal models.
Human trials to protect against noise trauma are promising but current results remain tentative.
Synaptopathy has emerged as an early event in NIHL and neurotrophins are potential rescue agents.
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Declaration of interest
J. Schacht is named as a co-inventor of ACEMg for treatment of hearing loss (US Patent 7,951,845 B2 to the University of Michigan), but is not involved in any trials testing this compound or any other commercial exploitation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.